This blog describes Metatime in the Posthuman experience, drawn from Sir Isaac Newton's secret work on the future end of times, a tract in which he described Histories of Things to Come. His hidden papers on the occult were auctioned to two private buyers in 1936 at Sotheby's, but were not available for public research until the 1990s.

Wednesday, September 18, 2013

Catastrophic failure or progressive decline? These are alternatives in cellular degeneration. For example, some cells, such as cancer cells, do not age. One commenter at Naked Science Forum notes: "some mutations which cause cancer are not actually causing excessive
cell division but a mutation upon the gene which controls programmed
cell death... so they don't die when they should and you thus end up
with accumulation."

Similarly, researchers have found a type of yeast that does not age (that is, it does not show cellular damage and wear as cells divide over time), but rather, it gets younger as its cells divide. These particular yeast cells do die, but as a result of sudden, catastrophic failure at any given moment, rather thanthrough a progressive decline.

Under favorable conditions, the microbe, a species of yeast called S. pombe, does not age the way other microbes do, the researchers said.

Typically, when single-celled organisms divide in half, one half
acquires the majority of older, often damaged cell material, while the
other half acquires mostly new cell material.

But in the new study, researchers found that under favorable, nonstressful growing conditions, S. pombe
(a single-celled organism) divided in such a way that both halves
acquired about equal parts of old cell material. "As both cells get only
half of the damaged material, they are both younger than before," study
researcher Iva Tolic-Nørrelykke, of the Max Planck Institute of Molecular Cell Biology and Genetics in Germany, said in a statement.

What's more, previous research has shown that when cells divide and
continuously pass on old cell material, the cells that get the old
material start to divide more slowly — a sign of aging. This has been
seen in microorganisms such E. coli and the yeast S. cerevisiae.

But in the new study, S. pombe cells showed no increase in the time it took for them to divide, the researchers said.

That's not to say that S. pombe cells don't die. Some cells
did die in the study, but the deaths occurred suddenly, as a result of a
catastrophic failure of a cellular process, rather than aging, the
researchers said.

The researchers said they are not arguing that any given component of S. pombecells are immortal.
If a particular component of a cell is followed for a long enough time,
the researchers believe the cell that harbors this component will
eventually die. But "the probability of this death will be constant
rather than increasing over time," the researchers wrote in the Sept. 12
issue of the journal Current Biology.

During unfavorable, stressful conditions, S. pombe cells
distribute old cell material unevenly, and the cells that inherited the
old material eventually died, the study found. Also, during stressful
conditions, S. pombe showed an increase in division time.

Although there's no way to know for sure why the researchers did not detect aging in S. pombe
under favorable conditions, one likely explanation is that the cellular
damage is being repaired at the same rate that it's being formed, said
Eric Stewart, a microbiologist at Northeastern University in Boston, who
was not involved in the study.

But just because the study researchers did not detect aging in
favorable conditions doesn't meant that it's not occurring. "They're
trying to show the absence of something," in this case, aging, Stewart
said. "Showing the absence of something is a nearly impossible
challenge," he said.

S. pombe growth under favorable conditions could potentially serve as a model of nonaging cell types, such as cancer cells, the researchers said.

Researcher Paul Davies - author of The Goldilocks Enigma- wrote a 2012 report for The Guardian to ask if cancer is actually a way that a multi-cellular organism can regress to the single-celled organism model, where cells do not seem to age. Thus, he postulates, cancer essentially reverses the normal course of evolution from single cell to multicellular organism, even as the disease reverses the clock on cell death processes. But the question remains: why does cancer do this? What purpose is an evolutionary reversal trying to serve? Davies and an Australian physicist, Charles Lineweaver, maintain that cancer de-evolves a sufferer of the disease at the cellular level. The disease serves to activate increasingly archaic genes in a body as it spreads. Lineweaver claims that cancer is a "default cellular safe mode." From The Guardian report:

In the frantic search for an elusive "cure", few researchers stand
back and ask a very basic question: why does cancer exist? What is its
place in the grand story of life? Astonishingly, in spite of decades of
research, there is no agreed theory of cancer, no explanation for why,
inside almost all healthy cells, there lurks a highly efficient cancer
subroutine that can be activated by a variety of agents – radiation,
chemicals, inflammation and infection.

Cancer, it seems, is
embedded in the basic machinery of life, a type of default state that
can be triggered by some kind of insult. That suggests it is not a
modern aberration but has deep evolutionary roots, a suspicion confirmed
by the fact that it is not confined to humans but is widespread among
mammals, fish, reptiles and even plants. Scientists have identified genes implicated in cancer
that are thought to be hundreds of millions of years old. Clearly, we
will fully understand cancer only in the context of biological history.

For most of Earth's
history, life was confined to single-celled organisms. Over time,
however, a new possibility arose. Earth's atmosphere became polluted by a
highly toxic and reactive chemical – oxygen – created as a waste
product of photosynthesis. Cells evolved ingenious strategies to either
avoid the accumulating oxygen or to combat oxidative damage in their
innards. But some organisms turned a vice into a virtue and found a way
to exploit oxygen as a potent new source of energy. In modern organisms,
it is mitochondria that harness this dangerous substance to power the
cell.

With the appearance of energised oxygen-guzzling cells, the
way lay open for the second major transition relevant to cancer – the
emergence of multicellular organisms. This required a drastic change in
the basic logic of life. Single cells have one imperative – to go on
replicating. In that sense, they are immortal. But in multicelled
organisms, ordinary cells have outsourced their immortality to
specialised germ cells – sperm and eggs – whose job is to carry genes
into future generations. The price that the ordinary cells pay for this
contract is death; most replicate for a while, but all are programmed to
commit suicide when their use-by date is up, a process known as
apoptosis. And apoptosis is also managed by mitochondria.

Cancer
involves a breakdown of the covenant between germ cells and the rest.
Malignant cells disable apoptosis and make a bid for their own
immortality, forming tumours as they start to overpopulate their niches.
In this sense, cancer has long been recognised as a throwback to a
"selfish cell" era. But recent advances in research permit us to
embellish this picture. For example, cancer cells thrive in low-oxygen
(even zero-oxygen) conditions, reverting to an earlier, albeit less
efficient, form of metabolism known as fermentation.

Biologists
are familiar with the fact that organisms may harbour ancient traits
that reflect their ancestral past, such as the atavistic tails or
supernumerary nipples some people are born with. Evolution necessarily
builds on earlier genomes. Sometimes older genetic pathways are not
discarded, just silenced. Atavisms result when something disrupts the
silencing mechanism.

Charles Lineweaver, of the Australian National University, and I have proposed a theory of cancer based on its ancient evolutionary roots.
We think that as cancer progresses in the body it reverses, in a
speeded-up manner, the arrow of evolutionary time. Increasing
deregulation prompts cancer cells to revert to ever earlier genetic
pathways that recapitulate successively earlier ancestral life styles.
We predict that the various hallmarks of cancer progression will
systematically correlate with the activation of progressively older
ancestral genes. The most advanced and malignant cancers recreate
aspects of life on Earth before a billion years ago.

Ancient genes
remain functional only if they continue to fulfill a biological
purpose. In early-stage embryo development, when the basic body plan is
laid down (also in low-oxygen conditions, incidentally) ancestral genes
help guide developmental processes before being switched off. Every
human, for example, possesses tails and gills for a time in the womb.
Significantly, researchers have recently identified examples of
early-stage embryonic genes being reawakened in cancer.

The deep
links between evolutionary biology, developmental biology and cancer
have huge implications for therapy, and also provide an unexpected
reason to study cancer. By unravelling the details of cancer initiation
and progression, scientists can open a window on the past through which
we can gain tantalising glimpses of life in a bygone age.

About Me

Welcome to my blog, dedicated to the aporia, anomie, mysteries, and nervous tensions of the turn of the Millennium. I'm a writer and academic, trained in the field of history. These are my histories of things that define the spirit of our times. This blog also goes beyond historians' visions of the past, and examines how metatime and time are perceived in other media and disciplines, between generations, and in high and pop culture.